{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T21:59:37Z","timestamp":1789077577790,"version":"build-2803163510"},"reference-count":162,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2022,10,31]],"date-time":"2022-10-31T00:00:00Z","timestamp":1667174400000},"content-version":"vor","delay-in-days":303,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100020598","name":"Multiple Sclerosis Society of Western Australia","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100020598","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clin &amp; Trans Imm"],"published-print":{"date-parts":[[2022,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Multiple sclerosis is associated with Epstein\u2013Barr virus (EBV) infection, B\u2010cell dysfunction, gut dysbiosis, and environmental and genetic risk factors, including female sex. A disease model incorporating all these factors remains elusive. Here, we hypothesise that EBV\u2010infected memory B cells (MBCs) migrate to gut\u2010associated lymphoid tissue (GALT) through EBV\u2010induced expression of LPAM\u20101, where they are subsequently activated by gut microbes and\/or their products resulting in EBV reactivation and compartmentalised anti\u2010EBV immune responses. These responses involve marginal zone (MZ) B\u00a0cells that activate CD4\n                    <jats:sup>+<\/jats:sup>\n                    T\u2010cell responses, via HLA\u2010DRB1, which promote downstream B\u2010cell differentiation towards CD11c\n                    <jats:sup>+<\/jats:sup>\n                    \/T\u2010bet\n                    <jats:sup>+<\/jats:sup>\n                    MBCs, as well as conventional MBCs. Intrinsic expression of low\u2010affinity B\u2010cell receptors (BCRs) by MZ B cells and CD11c\n                    <jats:sup>+<\/jats:sup>\n                    \/T\u2010bet\n                    <jats:sup>+<\/jats:sup>\n                    MBCs promotes polyreactive BCR\/antibody responses against EBV proteins (e.g. EBNA\u20101) that cross\u2010react with central nervous system (CNS) autoantigens (e.g. GlialCAM). EBV protein\/autoantigen\u2010specific CD11c\n                    <jats:sup>+<\/jats:sup>\n                    \/T\u2010bet\n                    <jats:sup>+<\/jats:sup>\n                    MBCs migrate to the meningeal immune system and CNS, facilitated by their expression of CXCR3, and induce cytotoxic CD8\n                    <jats:sup>+<\/jats:sup>\n                    T\u2010cell responses against CNS autoantigens amplified by BAFF, released from EBV\u2010infected MBCs. An increased abundance of circulating IgA\n                    <jats:sup>+<\/jats:sup>\n                    MBCs, observed in MS patients, might also reflect GALT\u2010derived immune responses, including disease\u2010enhancing IgA antibody responses against EBV and gut microbiota\u2010specific regulatory IgA\n                    <jats:sup>+<\/jats:sup>\n                    plasma cells. Female sex increases MZ B\u2010cell and CD11c\n                    <jats:sup>+<\/jats:sup>\n                    \/T\u2010bet\n                    <jats:sup>+<\/jats:sup>\n                    MBC activity while environmental risk factors affect gut dysbiosis. Thus, EBV infection, B\u2010cell dysfunction and other risk factors converge in GALT to generate aberrant B\u2010cell responses that drive pathogenic T\u2010cell responses in the CNS.\n                  <\/jats:p>","DOI":"10.1002\/cti2.1418","type":"journal-article","created":{"date-parts":[[2022,10,31]],"date-time":"2022-10-31T13:00:20Z","timestamp":1667221220000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["<scp>Epstein\u2013Barr<\/scp>\n                    virus infection, B\u2010cell dysfunction and other risk factors converge in gut\u2010associated lymphoid tissue to drive the immunopathogenesis of multiple sclerosis: a\u00a0hypothesis"],"prefix":"10.1002","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5674-8462","authenticated-orcid":false,"given":"Jonatan","family":"Leffler","sequence":"first","affiliation":[{"name":"Telethon Kids Institute University of Western Australia  Perth WA Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0210-3452","authenticated-orcid":false,"given":"Stephanie","family":"Trend","sequence":"additional","affiliation":[{"name":"Telethon Kids Institute University of Western Australia  Perth WA Australia"},{"name":"Perron Institute for Neurological and Translational Science University of Western Australia  Perth WA Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7207-6467","authenticated-orcid":false,"given":"Prue H","family":"Hart","sequence":"additional","affiliation":[{"name":"Telethon Kids Institute University of Western Australia  Perth WA Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4644-1982","authenticated-orcid":false,"given":"Martyn A","family":"French","sequence":"additional","affiliation":[{"name":"School of Biomedical Sciences University of Western Australia  Perth WA Australia"},{"name":"Immunology Division PathWest Laboratory Medicine  Perth WA 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